| Autor: |
Fu, Yuling, Wang, Peng, Zhao, Jingjing, Tan, Yunke, Sheng, Junli, He, Shitong, Du, Xialin, Huang, Yulan, Yang, Yalong, Li, Jinling, Cai, Yuxiong, Liu, Yuxuan, Hu, Shengfeng |
| Zdroj: |
Cell Death and Differentiation; 20210101, Issue: Preprints p1-14, 14p |
| Abstrakt: |
Deubiquitinases (DUBs) regulate diverse biological processes and represent a novel class of drug targets. However, the biological function of only a small fraction of DUBs, especially in adaptive immune response regulation, is well-defined. In this study, we identified DUB ubiquitin-specific peptidase 12 (USP12) as a critical regulator of CD4+T cell activation. USP12 plays an intrinsic role in promoting the CD4+T cell phenotype, including differentiation, activation, and proliferation. Although USP12-deficient CD4+T cells protected mice from autoimmune diseases, the immune response against bacterial infection was subdued. USP12 stabilized B cell lymphoma/leukemia 10 (BCL10) by deubiquitinating, and thereby activated the NF-κB signaling pathway. Interestingly, this USP12 regulatory mechanism was identified in CD4+T cells, but not in CD8+T cells. Our study results showed that USP12 activated CD4+T cell signaling, and targeting USP12 might help develop therapeutic interventions for treating inflammatory diseases or pathogen infections. |
| Databáze: |
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